Nazir afhganzai

2. DEFINITION
•RAPID DECREASE IN KIDNEY FUNCTION MOSTLY
REVERSIBLE
•RESULTING IN AN INABILITYTO MAINTAIN ACID-BASE,
FLUIDAND ELECTROLYTE BALANCE

3. DEFINITION
•AKI IS DEFINED AS AN ABSOLUTE INCREASE IN SERUM
CREATININE BY 0.3 MG/DL OR MORE WITHIN 48 HOURS
OR A RELATIVE INCREASE OF GREATER THAN OR EQUAL
TO 1.5 TIMES BASELINE TO HAVE OCCURRED WITHIN 7
DAYS

4. ACUTE KIDNEY INJURY
• CHARACTERIZED BY:
• URINE PRODUCTION IS LESS THAN 400–500 ML/DAY OR LESS THAN 20 ML/H
A. STAGE 1:1.0- TO 1.5-FOLD INCREASE IN SERUM CREATININE OR A DECLINE IN
URINARY OUTPUT TO LESS THAN 0.5 ML/KG/H OVER 6–12 HOURS
B. STAGE 2: 2.0- TO 2.9-FOLD INCREASE IN SERUM CREATININE OR DECLINE IN
URINARY OUTPUT TO LESS THAN 0.5 ML/KG/H OVER 12 HOURS OR LONGER
C.STAGE 3:3-FOLD OR GREATER INCREASE IN SERUM CREATININE, AN INCREASE IN
SERUM CREATININE TO GREATER THAN OR EQUAL TO 4 MG/DL, A DECLINE IN
URINARY OUTPUT TO LESS THAN 0.3 ML/KG/H FOR 24 HOURS OR LONGER, ANURIA
FOR 12 HOURS OR LONGER,

5. ETIOLOGY
•DIVIDED INTO THREE
CATEGORIES:
PRERENAL:55% PRERENAL AZOTEMIA
RENAL:40%
POSTRENAL:5%

6.  NEPHROTOXIC
DRUGS
EXOGENOUS
ENDOGENOUS:CALCIUM,MYOG
LOBIN,URATEOXALATE

7. PATHOPHYSIOLOGY

8. CLINICAL FEATURES
oMANY PATIENTS WILL NOT EXPERIENCE ANY SYMPTOMS
oUREMIA CAN CAUSE NAUSEA, VOMITING, MALAISE, AND
ALTERED SENSORIUM
oSYMPTOMS AND SIGNS OF THE UNDERLYING DISEASE
PROCESS CAUSING THEIR AKI (EG, SLE)
oHYPERTENSION
oARRHYTHMIAS DUE TO HYPERKALEMIA

9. CLINICAL FEATURES- CONTINUE
• NONSPECIFIC DIFFUSE ABDOMINAL PAIN AND ILEUS
• PERICARDIAL EFFUSIONS
• BLEEDING AND CLOTTING DISORDERS
• CONFUSION
• ASTERIXIS
• PHYSICAL FINDINGS:TACHYCARDIA,FEVER,ORTHOSTATIC HYPOTENSION
• DECREASED JUGULAR VENOUS PRESSURE

10. INVESTIGATIONS
LAB TESTS
oELEVATED SERUM CREATININE
oMETABOLIC ACIDOSIS
oHYPERKALEMIA
oANEMIA
oDIPSTICK TEST
oSPECIFIC GRAVITY
RADIOLOGIC
• ULTRASOUND
• CT SCAN
• MRI
• PYLOGRAPHY
• CONTRAST ANGIOGRAPHY

11. PYELOGRAPHY

12. CYSTOSCOPY

13. CONTRAST ANGIOGRAPHY

14. SPECIFIC GRAVITY

15. ECG CHANGES
•PEAKED T WAVES
•PR PROLONGATION
•QRS WIDENING
•HYPERPHOSPHATEMIA

16. DIFFERENTIAL DIAGNOSIS

19. COMPLICATIONS
UREMIA:ELECATION OF NITROGENOUS COMPOUNDS,ELEVATIONS OF BUN
AND CREATININE
HYPERVOLEMIA AND HYPOVOLEMIA:DECREASED SODIUM AND
FLUID EXCRETION
HYPERKALEMIA:OLIGOUREA AND DECREASED POTASSIUM EXCRETION
HYPONATREMIA:HYPOTONIC CRYSTALLOIDS
HYPERPHOSPHATEMIA :RHABDOMYOLYSIS,HEMOLYSIS

20. COMPLICATIONS
HYPOCALCEMIA:DECREASED PRODUCTION OF 1.25 HYDROXY VITAMIN
D,RESISTANCE TO PARATHYROID HORMONE
ACIDOSIS:DIABETIC KETOACIDOSIS,LACTIC ACIDOSIS,METABOLISM OF
PROTEINS
BLEEDING:PLATELET DYSFUNCTION,DECREASED ERYTHROPOEITIN
PRODUCTION
INFECTION:IV CANNULA,MECHANICAL VENTILATOR,FOLLEY
CATHETERIZATION
CARDIAC COMPLICATIONS:PERICARDITIS,CARDIAC TAMPONADE,ARRHYTHMIAS
MALNUTRITION:HYPERCATABOLIC STATE

21. TREATMENT
• SUPPORTIVE MEASURES:
• VOLUME MANAGEMENT
• HYPERVOLUMEIA
• HYPO AND
HYPERNATREMIA
• HYPERKALEMIA
• METABOLIC ACIDOSIS
• HYPERPHOSPHATEMIA
• HYPOCALCEMIA
• HYPERURECEMIA
• DIET
• ANEMIA
• GI BLEEDING
• INFECTION
• DIALYSIS INDICATIONS
AND MODALITIES

22. SPECIFIC TREATMENT
PRERENAL AK:
VOLUME REPLACEMENT FOR HYPOVOLEMIA
PACKED RBC IN ANEMIA
SALINE 0.9%
HEMODYNAMIC MONITORING BY CENTRAL VENOUS CATHETER
• REENAL AKI:
DISCONTINUING NEPHROTOTOXIC DRUGS
TREATING CAUSATIVE AGENT:PREDNISOLONE, 60MG/DAY ,FUROSEMIDE 200-400MG/DAY
• POSTRENAL AKI: FOLLEY CATHETERIZATION,CYSTOSCOPY,STENT INSERTION

23. DIALYSIS INDICATIONS

25. PROGNOSIS
• DEVELOPMENT OF AKI IS ASSOCIATED WITH:
a.IN-HOSPITAL AND LONG-TERM MORTALITY
b.LONGER LENGTH OF STAY
c.INCREASED COSTS
d.POSTRENAL AZOTEMIA CARRY A BETTER
PROGNOSIS THAN INTRINSIC AKI
e.10% MAY DEVELOP END-STAGE RENAL DISEASE